Anesthesia and analgesia
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Anesthesia and analgesia · Apr 2004
Neither the accuracy nor the precision of thermal dilution cardiac output measurements is altered by acute tricuspid regurgitation in pigs.
Whether measurement of cardiac output using the thermal dilution technique (TDCO) is valid in the presence of tricuspid regurgitation (TR) is controversial. We assessed the accuracy and precision of the technique in pigs by comparison with data from an electromagnetic flowmeter on the aorta (EMCO). TR was created with sutures that immobilized the free-wall leaflets of the tricuspid valve, and cardiac output was adjusted with dobutamine to give values comparable to control measurements. TR reduced forward stroke volume from 17.2 to 12.6 mL/beat and caused the right atrium to dilate and pulse in synchrony with the right ventricle. Acute TR did not affect the linear regression relation between TDCO and EMCO and did not alter the correlation coefficient (r = 0.94 during both control and TR). These data demonstrate that acute TR does not affect the accuracy or precision of TDCO in pigs. ⋯ Cardiac output is a valuable measurement that guides the medical care of patients with heart and lung disease. This study demonstrates that the thermal dilution technique of determining cardiac output is valid when acute tricuspid valve regurgitation is present in pigs.
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Anesthesia and analgesia · Apr 2004
The effects of alfentanil on cytosolic Ca(2+) and contraction in rat ventricular myocytes.
Previous investigations of the effects of potent opioid analgesics on the heart have concentrated on effects on contraction magnitude and time course, but little is known about their effects on cytosolic Ca(2+) regulation in cardiac tissue. In this study, we sought to assess the effects of alfentanil on contractility and the cytosolic Ca(2+) transient in ventricular myocytes isolated from the rat ventricle by enzymatic dispersion. Cells were loaded with fura-2 and electrically stimulated at 1 Hz, and Ca(2+) transients and contractions were recorded optically at 30 degrees C. Alfentanil 10(-8) and 10(-7) M had no effect on the magnitude or time course of contraction or the cytosolic Ca(2+) transient. In contrast, 10(-6) M alfentanil induced a significant (P < 0.001) positive inotropic effect, increasing the mean (+/-SEM) unloaded shortening from 7.3 +/- 1.3 microm to 8.7 +/- 1.4 microm (an increase of 20%), with no change in the cytosolic Ca(2+) transient. Myofilament Ca(2+) sensitivity was significantly (P = 0.027) increased by 10(-6) M alfentanil but unaffected at 10(-7) M alfentanil. These data show that 10(-6) M alfentanil, a concentration close to the maximum clinical free plasma concentration, induced a positive inotropic effect due to sensitization of the myofilaments to Ca(2+) rather than to modified cytosolic Ca(2+) regulation. ⋯ Alfentanil, at concentrations achieved in clinical practice, increased contraction in ventricular cells by a mechanism involving an increase in the sensitivity of the contractile apparatus to Ca(2+).
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Anesthesia and analgesia · Apr 2004
Isoflurane pretreatment supports hemodynamics and leukocyte rolling velocities in rat mesentery during lipopolysaccharide-induced inflammation.
We hypothesized that the protective effects of isoflurane (ISO) pretreatment on the vasculature may be attributed, in part, to altered leukocyte-endothelial interactions. Rats were anesthetized with pentobarbital and then randomized into four groups: control, ISO-control (pretreatment with 30 min of 1.4% ISO), lipopolysaccharide (LPS; 10 mg/kg IV), and ISO-LPS (ISO pretreatment and then LPS). The mesentery was prepared for intravital videomicroscopy. Mean arterial blood pressure (MAP), along with microcirculatory variables that included postcapillary venular and arteriolar blood flow velocity and leukocyte dynamics (number of rolling and adherent leukocytes and individual rolling leukocyte velocities), were measured hourly (baseline and at 0-4 h). In LPS rats, ISO pretreatment significantly (P < 0.05) attenuated the decrease in MAP at 2 and 4 h after LPS and increased leukocyte rolling velocities after 2-4 h. Four hours after LPS, leukocyte rolling velocities were >200% more rapid (63.7 +/- 27.6 microm/s versus 19.8 +/- 6.4 micro m/s) in ISO-LPS versus LPS rats. In control rats, ISO pretreatment had no effect on MAP or leukocyte rolling velocities but increased the number of rolling leukocytes. ISO pretreatment had no effect on arteriolar and postcapillary venular blood flow velocity in LPS rats or leukocyte adherence in LPS or control rats. In conclusion, ISO pretreatment supported hemodynamics and increased leukocyte rolling velocities but did not alter the number of rolling or adherent leukocytes in the mesenteric microcirculation during LPS-induced inflammation. ⋯ Isoflurane pretreatment supported hemodynamics and increased leukocyte rolling velocities in the mesenteric microcirculation during lipopolysaccharide-induced inflammation. Faster rolling velocities may reduce the incidence of inflammation by decreasing leukocyte-endothelial interactions and cellular injury.
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Anesthesia and analgesia · Apr 2004
Intrathecal morphine reduces infarct size in a rat model of ischemia-reperfusion injury.
Systemically-administered morphine reduces infarct size in rat models of myocardial ischemia-reperfusion. We sought to determine whether much smaller doses of spinally-administered morphine offer a similar cardioprotective benefit. Barbiturate-anesthetized, open-chested, Wistar rats with chronic indwelling thoracic intrathecal catheters were instrumented for hemodynamic measurements and subjected to 30 min of coronary occlusion and 90 min of reperfusion. Myocardial infarct size was determined using triphenyl-tetrazolium staining. Rats were randomly assigned to receive intrathecal (IT) 0.9% saline (vehicle), IV morphine (0.3 mg/kg) plus IT saline, small-dose IT morphine (0.3 microg/kg), or large-dose IT morphine (3 microg/kg) 20 min before occlusion. IV and both doses of IT morphine reduced infarct size, defined as area of necrosis expressed as a percentage of area at risk (%AN/AAR), as compared with vehicle. The %AN/AAR group means were as follows: IV (n = 7), 30% +/- 6%; IT(small-dose) (n = 9), 30% +/- 5%; IT(large-dose) (n = 9), 18% +/- 4%; and vehicle (n = 10), 47% +/- 5%. There were no significant differences in infarct size among the morphine-pretreated rats. During ischemia-reperfusion, heart rate was unchanged from baseline in the IT(large-dose) group, whereas in the IT(small-dose), IV and vehicle groups, significant declines in heart rate occurred. Changes in arterial blood pressure were similar among groups. These results indicate that IT morphine reduces infarct size in rats, and this benefit is as great as that provided by IV morphine administration. ⋯ Our findings suggest that spinally-administered morphine provides a previously unrecognized cardioprotective benefit. In anesthetized rats subjected to ischemia-reperfusion injury, we show that very small doses of intrathecal morphine reduce infarct size in rats, and this benefit is as great as that provided by much larger doses of IV morphine.